ArticleMolecular and cellular biochemistry2009
Role of inositol polyphosphates in programmed cell death.
Article in Molecular and cellular biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- The Underlying Mechanisms and Emerging Strategies to Overcome Resistance in Breast Cancer.Cancers · 2025Review
- Encapsulation of Inositol Hexakisphosphate with Chitosan via Gelation to Facilitate Cellular Delivery and Programmed Cell Death in Human Breast Cancer Cells.Bioengineering (Basel, Switzerland) · 2024Article
- Inositol Hexaphosphate in Bone Health and Disease.Biomolecules · 2024Review
- Guar-Based Injectable Hydrogel for Drug Delivery and In Vitro Bone Cell Growth.Bioengineering (Basel, Switzerland) · 2023Article
- The Metabolite Content of the Post-Culture Medium of the Tree FernInternational journal of molecular sciences · 2022Article
- CRISPR/Cas9 mediated disruption ofJournal of advanced research · 2022Article
- Article
- Integration of Transcriptomics and Metabolomics to Reveal the Molecular Mechanisms Underlying Rhodium Nanoparticles-Based Photodynamic Cancer Therapy.Pharmaceutics · 2021Article
- Pontocerebellar hypoplasia due to bi-allelic variants in MINPP1.European journal of human genetics : EJHG · 2021Article
- Role of inositol polyphosphates in programed cell death in Dictyostelium discoideum and its developmental life cycle.Molecular and cellular biochemistry · 2018Article
- Molecular characterization, modeling, and docking analysis of late phytic acid biosynthesis pathway gene,3 Biotech · 2018Article
- Endoplasmic reticulum stress-induced apoptosis accompanies enhanced expression of multiple inositol polyphosphate phosphatase 1 (Minpp1): a possible role for Minpp1 in cellular stress response.Cell stress & chaperones · 2016Article
- Interdependence of DNA mismatch repair proteins MLH1 and MSH2 in apoptosis in human colorectal carcinoma cell lines.Molecular and cellular biochemistry · 2016Article
- Conformational stability of inositol 1,3,4,5,6-pentakisphosphate 2-kinase (IPK1) dictates its substrate selectivity.The Journal of biological chemistry · 2013Article
- Conformational changes in inositol 1,3,4,5,6-pentakisphosphate 2-kinase upon substrate binding: role of N-terminal lobe and enantiomeric substrate preference.The Journal of biological chemistry · 2012Article
- Detection of DNA mismatch repair proteins in fresh human blood lymphocytes--towards a novel method for hereditary non-polyposis colorectal cancer (Lynch syndrome) screening.Journal of experimental & clinical cancer research : CR · 2011Article
- Changes in cellular levels of inositol polyphosphates during apoptosis.Molecular and cellular biochemistry · 2010Article
- Inositol 1,3,4,5,6-pentakisphosphate 2-kinase is a distant IPK member with a singular inositide binding site for axial 2-OH recognition.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Crystallization and preliminary X-ray diffraction analysis of inositol 1,3,4,5,6-pentakisphosphate kinase from Arabidopsis thaliana.Acta crystallographica. Section F, Structural biology and crystallization communications · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of inositol polyphosphates (InsPs) in the mediation of cellular apoptosis was investigated in mouse MC3T3 osteoblastic cell line. Extracellular administration of InsP(4), InsP(5), and InsP(6) increased apoptosis in a dose-dependent manner. InsP(6) was more potent than InsP(5) and InsP(4) in promoting apoptosis. Inositol hexasulfate (InsS(6)), a structural analog of InsP(6), was used to determine specificity of InsP(6)-induced apoptosis as measured by acridine orange/ethidium bromide, flow cytometry, and DNA degradation. In order to study the effects of endogenous InsPs on apoptosis, we used NaF and antimycin A as treatment agents to manipulate intracellular levels of InsPs. NaF is known to increase levels of higher InsPs by inhibiting InsPs phosphatases, a process that is reversed by antimycin A because InsPs kinases are inhibited as a result of depletion of cellular ATP pools. Apoptosis was induced in MC3T3 cells in a NaF dose- and time-dependent manner. Approximately 50% apoptosis was observed at 1 mM NaF in 8 h. Prior treatment with 10 microM antimycin A for 30 min significantly reduced the NaF-induced apoptosis as compared with its control. Additionally, we measured changes in AKT phosphorylation, cleavage of caspase-3 and caspase-9, and release of cytochrome C from mitochondria into cytosol. These changes coincided with total cellular InsPs under similar conditions. The data indicated that NaF-induced changes in apoptotic markers could be due to an increased endogenous InsPs that were partially reversed by antimycin A treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.